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Journal of Neurology and Neuroscience

  • ISSN: 2171-6625
  • Journal h-index: 18
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Abstract

Running Head: Craniopharyngioma and Immune Response

Martha Lilia TS, Citlaltepelt SL, Ma. Elena HC, Carlos SG and Manuel CL

Background: Craniopharyngioma is a rare tumor and accounts for 5-10% of childhood tumors and, despite of the benign histological features, few studies on inflammatory cells and response in craniopharyngioma have been published.

The aim of this word was to known about inflammation and immunoresponce in Craniopharyngiomas, which were evaluated thought immunohistochemistry. HIF1a, IFI16, TNF-α, TNF- λ, HMC-2, interleukins 6, CD4, CD20, CD68, CD57, Fascin, plasma cells were used. Tumors were divided between recurrence vs no recurrence and brain infiltration.

Methods and materials: We retrospectively evaluated clinico-pathological findings in 56 patients with craniopharyngioma (CP). Based on histopathological and immunohistochemical findings and on clinical presentation, tumor size and follow-up data were correlated with emphasis in the inflammatory response.

Results: 45 were adamantinomatous craniopharyngiomas and 11 were papillary craniopharyngiomas. Inflammation was higher in the adamantinomatous type than in the papillary type and was associated with gliosis, dystrophic calcification, and wet keratin formation, as well as tumour size and the duration of patients’ follow-up. There was a statistically significant correlation between inflammation in craniopharyngioma and CD4 (p=0.041), CD20 (Phi=0.652, p=0.000), CD68 (Phi=0.493, p=0.000), NK (Phi=0.456, p=0.040) MHC-II (Phi=0.476, p=0.014), and IFI-16(Phi=0.436, p=0.031). However, there was no correlation between IL-6 immunoexpression and inflammation. Cases with more severe inflammation were associated with a shorter follow-up period than cases in which no inflammation was present (Log Rank text p=0.07, IC95%).

Conclusions: These data suggest that macrophages and inflammatory response may act as activators in craniopharyngiomas. This may be involved in tumor cell proliferation and malignant transformation. Understanding the mechanism of these differences may be critical in the development of novel immunotherapies for CP, as a treatment strategy for CP and to illustrate possible physiological pathways responsible for the therapeutic benefit observed. Further studies are needed.